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Kolaviron attenuates diclofenac-induced nephrotoxicity in male Wistar rats

Alabi, Quadri K., Akomolafe, Rufus O., Adefisayo, Modinat A., Olukiran, Olaoluwa S., Nafiu, Aliyat O., Fasanya, Micheal K., Oladele, Ayowole A.
Applied physiology, nutrition and metabolism 2018 v.43 no.9 pp. 956-968
Garcinia kola, animal models, anorexia, anti-inflammatory activity, catalase, cations, creatinine, diclofenac, excretion, flavonoids, food intake, glucose, glutathione, histopathology, hydrogen peroxide, ketone bodies, kidneys, laboratory animals, males, malondialdehyde, necrosis, nephrotoxicity, potassium, propylene glycol, prostaglandins, rats, renal failure, renoprotective effect, seeds, sodium, superoxide dismutase, urea, urine
The beneficial effects of kolaviron, a natural biflavonoid from the seeds of Garcinia kola, have been attributed to its antioxidant and anti-inflammatory activities. This study was designed to investigate the renoprotective effect of kolaviron in rat model of diclofenac (DFC)-induced acute renal failure. Thirty-five male Wistar rats were divided into 7 groups of 5 rats each as follows: a control group that received propylene glycol orally and treatment groups that received DFC, DFC recovery, DFC followed by kolaviron at 3 different doses, and kolaviron only. DFC-treated rats showed sluggishness, illness, and anorexia. Their urine contained appreciable protein, glucose, and ketone bodies. Histopathological examination of their kidneys revealed profound acute tubular necrosis. DFC treatment significantly increased levels of plasma creatinine, urea, sodium, chloride, potassium ions, and increased renal tissue activities of superoxide dismutase, catalase, levels of malondialdehyde, and hydrogen peroxide. Fractional excretion of sodium and potassium and renal tissue levels of reduced glutathione and prostaglandin E₂ (PGE₂) decreased significantly in DFC-treated groups. However, kolaviron administration significantly reduced the toxic effect of DFC on PGE₂ release; plasma levels of creatinine, urea, glucose, and electrolytes; and significantly attenuated renal tubular and oxidative damages. Furthermore, the effects of DFC administration on food consumption, water intake, urine output and urine protein, glucose, ketone bodies, and electrolytes were significantly attenuated in animals treated with kolaviron. The results suggested that kolaviron ameliorated DFC-induced kidney injury in Wistar rats by decreasing renal oxidative damage and restoration of renal PGE₂ release back to the basal levels.